Keshan disease is a potentially fatal cardiomyopathy in humans. Selenium deficiency, T-2 toxin, and myocarditis virus are thought to be the major factors contributing to Keshan disease. But the relationship among these three factors is poorly described. This study aims to explore whether selenium deficiency aggravates T-2 toxin-induced cardiomyocyte injury and its underlying mechanism. Cardiomyocytes were isolated from neonatal rat and cultured at the physiological (2.0 μM) or lower concentrations of selenium with different concentrations of T-2 toxin. Our results showed that selenium deficiencies aggravated T-2 toxin-induced cardiomyocyte injury in a concentration-dependent manner as demonstrated by MTT bioassay, LDH activity, reactive oxygen species levels and caspase 3 protein expressions. T-2 toxin treatment significantly increased mRNA expressions for stress proteins GRP78 and CHOP in cardiomyocytes compared with the control. Selenium deficiencies further promoted GRP78, CHOP and p-eIF2α expressions. Knockdown of CHOP by the specific small interfering RNA eliminated the effect of selenium deficiencies on T-2 toxin-induced injury. It could be concluded that selenium deficiency aggravates T-2 toxin-induced cardiomyocyte injury through initiating more aggressive endoplasmic reticulum stress.

克山病是人类潜在的致命性心肌病。硒缺乏，T-2毒素和心肌炎病毒被认为是导致克山病的主要因素。但是，这三个因素之间的关系描述得很少。这项研究旨在探讨硒缺乏是否会加剧T-2毒素诱导的心肌细胞损伤及其潜在机制。从新生大鼠中分离心肌细胞，并在生理（2.0μM）或更低浓度的硒中加入不同浓度的T-2毒素进行培养。我们的结果表明，硒缺乏会以浓度依赖的方式加重T-2毒素诱导的心肌细胞损伤，如MTT生物测定法，LDH活性，活性氧水平和caspase 3蛋白表达所证明的。与对照组相比，T-2毒素处理显着增加了心肌细胞中应激蛋白GRP78和CHOP的mRNA表达。硒缺乏症进一步促进了GRP78，CHOP和p-eIF2α的表达。通过特定的小分子干扰RNA来减少CHOP消除了硒缺乏对T-2毒素诱导的损伤的影响。可以得出结论，硒缺乏会通过引发更具侵略性的内质网应激而加剧T-2毒素诱导的心肌细胞损伤。